Hypokalemia is a common electrolyte disorder. Transient causes of hypokalemia are due to cell shift, whereas sustained hypokalemia is caused by either inadequate intake or excessive potassium loss. Evaluation of the intake, distribution, and excretion of potassium should include the following: (1) a careful history, including use of drugs, medications, and the presence of vomiting or diarrhea; (2) physical examination, including orthostatic changes in blood pressure and heart rate; and (3) measurement of urine and plasma electrolytes. Urinary potassium wasting is caused by pathophysiologic conditions that couple increased distal sodium delivery with increased plasma aldosterone levels or aldosterone-like effects. If urinary potassium loss is identified, the next step is to determine whether the loss is caused by a primary increase in distal delivery of sodium or a primary increase in mineralocorticoid level. A primary increase in distal delivery should be associated with volume depletion, whereas a primary increase in mineralocorticoid level generally is associated with volume expansion and hypertension. In patients with a primary increase in mineralocorticoid activity, it is useful to measure plasma renin activity and plasma aldosterone levels. Complications of hypokalemia include muscle weakness, rhabdomyolysis, cardiac arrhythmias, impaired urinary concentrating ability, and glucose intolerance.